Background: Non-small cell lung cancer (NSCLC) has a poor prognosis and is the most common cause of cancer-related deaths worldwide. Aminoacylase 1 (ACY1) plays a promoting role in some cancers, but its role in NSCLC is still unclear. Methods: Immunohistochemistry, Reverse transcription-polymerase chain reaction (RT-PCR) and western blotting assays were used to determine ACY1 expression patterns in NSCLC tissues and cell lines. The clinical significance of ACY1 in NSCLC was evaluated by χ 2 test and Kaplan-Meier analysis. MTT, flow cytometry, wound healing, and Transwell assays were performed to assess cell growth, apoptosis, migration, invasion, and tumorigenesis under different treatments. Male athymic BALB/C nude mice were used for xenotransplantation experiments.Results: The results showed that ACY1 expression was elevated in NSCLC tissue samples and cells, and high ACY1 expression predicted an advanced clinical process and shorter overall survival in patients with NSCLC. Overexpression of ACY1 significantly increased cell growth, migration, invasion, and tumorigenesis, and reduced cell apoptosis, indicating that ACY1 functions as an oncogene in NSCLC.Moreover, ACY1 decreased phosphatase and tensin homolog (PTEN) expression, increased its ubiquitination, and activated PI3K/AKT signaling. Overexpression of PTEN diminished the effects of ACY1 upregulation on cell tumorigenesis promotion.Conclusions: This study reveals that ACY1 may promote the progression of NSCLC via activating PI3K/AKT signaling in a PTEN-dependent manner. Our study may provide a better understanding of the pathogenesis and development of NSCLC.

Background: The identification of prognostic genes that can distinguish the prognostic risks of cancer patients remains a significant challenge. Recent studies show that long noncoding RNAs (lncRNAs) might act as prognostic biomarkers in a variety of cancers. This study aimed to identify and assess a prognostic lncRNA signature in patients with colon adenocarcinoma (COAD). Methods: We downloaded expression profiles and corresponding clinicopathological data from The CancerGenome Atlas (TCGA) database. We selected samples with lncRNA expression data and relevant clinical prognostic data for subsequent analysis. The association between lncRNA and prognostic function was analyzed by Cox regression analysis. The potential biofunctions of target lncRNA were investigated through bioinformatic analysis.Results: LncRNAs expression profiles and corresponding clinicopathological data of 480 COAD patients and 41 normal samples were obtained from TCGA database. A multivariate Cox analysis model was used to identify the lncRNA signature. AC010973.2 lncRNA was found to be significantly related to the survival of COAD patients. The area under the curve (0.758) and the C-index (0.753) further confirmed the prediction accuracy of our model. Through nucleic acid sequence comparison and literature search, we found that the homologous host gene SLC4A2 of AC010973.2 is significantly related to COAD. Conclusions:We provide here a new biomarker for COAD diagnosis and a new direction for further research on the pathogenesis of COAD.

Radiation induces submandibular gland damage by affecting Cdkn1a expression and regulating expression of miR-486a-3p in a xerostomia mouse model.